Becaria Angelica, Lahiri Debomoy K, Bondy Stephen C, Chen DeMao, Hamadeh Ali, Li Huihui, Taylor Russell, Campbell Arezoo
Department of Community and Environmental Medicine, Center for Occupational and Environmental Health Sciences, University of California, Irvine, Irvine, CA 92697-1825, USA.
J Neuroimmunol. 2006 Jul;176(1-2):16-23. doi: 10.1016/j.jneuroim.2006.03.025. Epub 2006 May 11.
Inflammatory and oxidative events are up-regulated in the brain of AD patients. It has been reported that in animal models of AD, exposure to aluminum (Al) or copper (Cu) enhanced oxidative events and accumulation of amyloid beta (Abeta) peptides. The present study was designed to evaluate the effect of a 3-month exposure of mice to copper sulfate (8 microM), aluminum lactate (10 or 100 microM), or a combination of the salts. Results suggest that although Al or Cu may independently initiate inflammatory or oxidative events, they may function cooperatively to increase APP levels.
在阿尔茨海默病（AD）患者的大脑中，炎症和氧化反应上调。据报道，在AD动物模型中，暴露于铝（Al）或铜（Cu）会增强氧化反应以及β淀粉样蛋白（Aβ）肽的积累。本研究旨在评估小鼠暴露于硫酸铜（8微摩尔）、乳酸铝（10或100微摩尔）或这两种盐的组合3个月后的影响。结果表明，尽管Al或Cu可能独立引发炎症或氧化反应，但它们可能协同作用以增加淀粉样前体蛋白（APP）水平。
